In the early 1990's, the present inventor introduced a low-frequency, low-intensity ultrasound device (“Hydrosound”) to effect microscopic cleaning of nursing-home patients during their weekly bathing-cycle. The preferred ultrasonic center frequency was 30 kHz and the maximum acoustic intensity was limited to 3 W/cm2, spatial peak temporal peak (SPTP). The 30 kHz center frequency was swept between 29 and 31 kHz at a rate of 120 Hz to avoid acoustic standing waves within the bathtub.
Ultrasonic human patient cleaning devices are known from U.S. Pat. No. 4,942,868, No. 5,048,520, No. 5,178,134, and No. 5,305,737. Subaqueous human application of the high frequency therapy devices is described in “CLINICS IN DIAGNOSTIC ULTRASOUND 16, edited by Wesley L. Nyborg, Marvin C. Ziskin—Section 11, Therapeutic Applications of Ultrasound, Mary Dyson.
Over the past ten years, thousands upon thousands of subaqueous exposures have demonstrated the overall safety of these ultrasonic exposure parameters for full-immersion cleaning of human patients having intact tissue with no open wounds. The only use-prohibition of the low-frequency, low-intensity ultrasound device was for wound therapy because at a frequency of 30 kHz and average acoustic intensity of more than 0.5 W/cm2 (SPTP), the device produced both inertial and transient cavitation events. Inertial or transient cavitation that occurred within 15 cm of the cleaning device's transducer demonstrated that this version of an ultrasonic cleaning modality could damage open wounds. Nevertheless, accepting this limitation, the FDA listed the low-frequency, low-intensity ultrasound device as a medical device equivalent to hydromassage or whirlpool devices but suitable for only cleaning human patients who have intact tissue without the presence of open wounds.
High-intensity ultrasound (not appropriate to this invention) can expand a bubble so rapidly during a negative-pressure cycle that the bubble collapses before it has a chance to shrink during the positive-pressure cycle. At high intensity, therefore, bubbles can grow rapidly in the course of one cycle of sound to the state of inertial cavitation collapse.
In what is known as Rectified Mass Diffusion, a bubble's size oscillates in phase with the acoustic pressure expansion (rarefaction) and compression cycles. The surface area of a bubble produced by ultrasound pressure is slightly greater during rarefaction than in compression cycles. Since the amount of gas that diffuses in or out of the bubble depends on the bubble's surface area and skin thickness, diffusion into the bubble during rarefaction cycles will be slightly greater than diffusion out during compression cycles. For each cycle of sound, the bubble expands a little more than it shrinks. Over many cycles the size of bubbles will grow slowly. With Rectified Mass Diffusion, the growing bubble can eventually reach applied frequency resonant size where it will most efficiently absorb energy from the ultrasound.
At 30 kHz, for example, the resonant bubble diameter is 100 microns while the critical bubble size, where the bubble can no longer absorb acoustic energy, is roughly 120 microns in diameter. After reaching resonant size, critical bubble size can be attained in a few more cycles of sound. When this occurs, liquid inertial force will rush into the bubble and implode it. Thus, within a few microns radius, the resulting implosion generates temperatures of thousands of degrees Kelvin and increases in pressure of thousands of atmospheres. This implosion phenomena is known as inertial or transient cavitation.
Also, when a bubble reaches a critical radius Rc at the same time that Blake's critical threshold pressure is reached, unstable bubble growth and therefore transient cavitation occur, with bubble collapse results similar to inertial cavitation. However, this particular phenomenon is subject to there being sufficient time in each pressure cycle to permit bubble growth. This is determined by the relationship between the radian frequency w of the imposed oscillations and the natural frequency wN of the bubble at its current size. If the radian frequency w is much less than the natural frequency wN then the liquid inertia is relatively unimportant in the bubble dynamics and Blake's threshold pressure criteria will hold and transient cavitation will ensue. On the other hand, if the radian frequency w is much greater than the natural frequency wN, the issue will involve the dynamics of bubble growth since its inertia will determine the size of bubble perturbations.
Inertial or transient cavitation (bubble) phenomena are manifested through the dynamic interaction of many diverse physical parameters, including the relationship between the frequency w of the imposed oscillations and the natural frequency wN of the bubble, the relationship between the pressure oscillation amplitude and the mean pressure, and whether the bubble is predominantly vapor filled or gas filled. Stable oscillations are more likely with predominantly gas filled bubbles, while bubbles that contain mostly vapor will more readily exhibit transient cavitation. Other variables that have a bearing are bubble temperature, thermal damping, water purity, surface tension, viscosity, viscous damping and radiation damping.
The probability that bubbles will oscillate stably or deteriorate into inertial or transient cavitation can be forecast mathematically if appropriate values are assigned to the above variables. Such mathematical analyses and treatises have value only post-mortem or in situations where water quality and temperature can be formulated before ultrasonic irradiation of an aqueous solution.
Unfortunately, to effect cavitation control in most patient treatment environments, water quality and its temperature control have to be viewed as an amorphous mass whose critical second-order parameters are not known and cannot be formulated beforehand. Only through experimentation can the cavitation tendency of this amorphous mass be established and only by experiment can the required ratio be determined between positive and rarefaction pressure cycles needed to predictably extend the time before a cavitation bubble implodes. Fortunately, the resulting states of cavitation from such manipulations can be determined by detecting the different acoustic pressure emission from stable and inertial/transient cavitation.
On the assumption that a human patient cleaning device would only be used for patients having intact tissue without open-wounds, it was sufficient to lower its applied ultrasonic intensity until occasional tingly-sensation events from transient cavitation in the vicinity of the patient, could be tolerated by the epidermis protected corium.
As implied above, there is a need for an ultrasound treatment device for open-wound therapy, where the body's external protective covering has broken down. On the assumption that low-frequency, low-intensity ultrasound device would only be used for patients having intact tissue, without the presence of open-wounds, standard hospital whirlpool disinfection procedures used for bathtub-cleaning after patient bathing have been judged sufficient. However, where the low-frequency, low-intensity ultrasound device is to be used with patients or subjects having open wounds, it will be critical for it to incorporate an automatic therapy tank decontamination means for killing shed pathogens between patients or subjects experiencing sonic open-wound treatments.
It is well-understood by medical-researchers that the biological basis of ultrasonic non-thermal therapy for beneficial cellular, tissue changes and wound healing depends on the presence of stable cavitation and associated microstreaming without the presence of inertial or transient cavitation. They also agree that the gas bubbles involved in transient/inertial cavitation undergo irregular oscillations and then implode, producing increases in temperature of thousands of degrees Kelvin and increases in pressure of thousands of atmospheres, localized in regions of only a few microns radius. They also recognize that any live cells exposed to such conditions would clearly be destroyed.
Side by side experiments on humans have shown that at ultrasonically treated wound sites there is an increase in total area of the blood vessels in the sections examined for both low and high frequency irradiation. There were more endothelial cells present following kHz treatment than following mHz treatment. This was particularly clear 7-days following ultrasound treatment; similar but undocumented favorable results were obtained for animals.
Several animal trials have been published in which mice, rabbits and pigs were subjected to 30 kHz low intensity ultrasound to establish the degree to which their lung tissue was damaged at increasing score levels of acoustic pressure amplitude, (0, 2, 4, 6, 8, 10, where 0 score was no damage and 10 score was death). To establish the level of ultrasound pressure vs. lung damage, 30 kHz ultrasound was propagated through thoroughly filtered water so as to eliminate the possibility of cavitation occurring or attenuation of the applied ultrasonic pressure waves. At approximately 145 kPa for 10-minutes, (8-10 score), the lungs of all the mice involved (more than 270) experienced massive lung-hemorrhage, followed by death. Subsequently, another experiment repeated the same ultrasonic exposure but this time in the presence of ultrasonic vibrating bubbles. Two mice were exposed to lethal amounts of ultrasound, (145 kPa for 10-minutes); both mice had lung damage scores of 0. A third mouse was exposed at 200 kPa and a fourth at 240 kPa and those also had lung damage scores of 0.
Because of the ability of fish to detect very low levels acoustic pressure amplitude it is very important to appreciate that the 0 kPa score clinical condition for mice was a sham condition where no ultrasound exposure was applied. It follows that when the mice were exposed to lethal levels of acoustic pressure (in excess of 145 kPa) in the presence of stable vibrating bubbles, as established by follow-on post mortems, their clinical condition was the same as the mice who received no ultrasound exposure, i.e., “alive, no lesions in lungs; normal respiration; no blood in chest cavity. No lung tissue damage; lung septa and capillaries (blood vessels) are normal.” The lung damage effect on humans, rabbits and pigs was far less than on mice; the lung is considered one of the most sensitive organs to the harmful effects of ultrasound exposure.
According to Hastings, (1990), a Sound Pressure Level (SPL) greater than 0.032 kPa is not harmful to fish. A Sound Pressure Level (SPL) greater than 1 kPa is harmful to many fish. According to Norris and Mohl, (1983), a Sound Pressure Level (SPL) greater than 266 kPa is fatal to most fish.